Post Cycle Therapy Topics and Facts

[LuvMuhRoids]

Below are topics I find most asked or discussed about PCT that I hope are beneficial and informative as possible.

[LuvMuhRoids]

Nolva is the dominating SERM in pct. Both nolva and clomid are SERMS but tissue specific or selective to certain areas. The case of clomid v nolva is clomid is a weak anti-estrogen blocker as opposed to nolvadex but clomid is needed to stimulate LH levels back to normal thus it's specific use. Nolvadex is selective in this aspect that it's main purpose as studies show is a weak estrogen and binds to receptors during PCT.

Nolvadex is needed for what I call the estrogen back lash one will recieve during the off time right after a cycle. When androgen levels drop estrogen flushs the receptors and nolvadex is needed. To not hinder gains or keep them longer, it is suggestable to restore the balance as quick as possible. Clomid is suggestable for this even though clomid is an anti-estrogen as well this is shown to be not it's selection.

To conclude, both SERMS are neccessary for proper restoration and serve both purposes needed in PCT. One, clomid to restore LH levels back to normal. Two, nolvadex to act as the anti-estrogen and block the flush.

I would like to add also this link to another article I have written that explains more in detail the case of clomid and nolvadex.

http://www.bigdogbodybuilding.com/showthread.php?t=99

LMR

[LuvMuhRoids]

My post cycle therapy consists of a three compound administration which is designed so that there is a primary and secondary LH stimulator which both are maximizing potential early in the duration; with the primary being phased out in extended protocol. With the addition of an Aromatase Inhibitor, which makes the above possible, the individual will also endure less of an increase in Sex Hormone Binding Globulin, which allows free testosterone levels to reach base line at a much quicker pace. The individual will also see less of a problem in most cases with sexual libido as the bounding SHBG is controlled(to an extent). Below you will find my suggested bare minimum, as well as a sample of an extended protocol. Extended PCT protcol is cycle length dependant so the below is not the standard for all cycles


PCT for cycles 8-16wks:
Day 1-30- .25mg L-dex + 100mg Clomid + 20mg Nolva

Extended protocol sample for a 12+ month cycle:
Day 1-15_ .25mg L-dex + 100mg Clomid + 20mg Nolva
Day 16-45_.25mg L-dex + 75mg Clomid + 20mg Nolva
Day 46-65_.25mg L-dex + 20mg Nolva
Day 66-80_.25mg L-dex

Now IMO, selective estrogen receptor modulators(SERMs) such as Clomiphine and Tamoxifen are selective to which tissues they bind too. Clomid being selective to the suprapituitary, while Tamox is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur.
With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual PCT duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

1. Nolva acts as the preventive measure to the estrogen flux
occured PC while clomid is the primary LH stimulator(Even more so in the case an AI is not used).
2. If your running a longer PCT, clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary. In the longer forms of PCT, the clomid will be phased out, leaving Nolva and L-dex

Arimidex(or L-dex)
Estrogen is the main inhibitence of restoring HPTA, and AI administration has been shown to increase gonadotrophin concentrations and serum Testosterone by up to 50%. In addition, by adding L-dex, the inhibitence of excess estrogen allows Tamox to work greater at LH stimulation in the begining stages of PCT, since the need to prevent binding in the mammery is lessened by the reduction in estrogen biosynthesis



Tamox vs Clomid

Am J Physiol 1983 Feb;240(2):E125-30

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

Adashi EY, Hsueh AJ, Bambino TH, Yen SS.

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

__________________________________________________
_________

Br J Pharmacol 1978 Apr;62(4):487-93

Differential depletion of cytoplasmic high affinity oestrogen receptors after the in vivo administration of the antioestrogens, clomiphene, MER-25 and tamoxifen.

Kurl RN, Morris ID.

1 The in vivo actions of the oestrogen antagonists, MER-25 and tamoxifen upon the cytosol oestrogen receptors prepared from amygdala, hypothalamus, pituitary and uterus of rats were studied 24 h after drug administration. 2 There was a dose-related depletion of cytosol oestrogen receptors. However, the uterine and pituitary receptors were consistently affected at a lower dose than were those from the brain. 3 The ratios of the combined central ED50 to the combined peripheral ED50 were clomiphene 169 greater than MER-25 19.2 greater than tamoxifen 2.13. 4 The receptor changes were not related to biological activity monitored by serum luteinizing hormone levels and uterotrophic response. 5 The possible role of these drug effects in the induction of ovulation and future developments are discussed.

__________________________________________________
__________

the following study was not available in my library, so i wasn't able to obtain the article or abstract. it may have to be purchased, so if someone is interested, here's the title and authors of the research.

Nippon Funin Gakkai Zasshi 1978 Oct;23(4):398-404

[The hormonal dynamics picture of tamoxifen treatment cases, in comparison of clomid treatment cases]

__________________________________________________
_______

Cochrane Database Syst Rev 2000;(2):CD000151

Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.

Vandekerckhove P, Lilford R, Vail A, Hughes E.

Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN.



Case for Clomid

J Clin Endocrinol Metab 1985 Nov;61(5):842-5

Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men.

Winters SJ, Troen P.

To examine the mechanism by which endogenous estrogens inhibit gonadotropin secretion in men, blood samples were drawn every 10 min for 12 h in five men before and at the completion of 3 weeks of treatment with the estrogen antagonist clomiphene citrate (50 mg twice daily). Samples were analyzed for LH and alpha-subunit by RIA. Clomiphene produced a 3-fold rise in circulating LH levels, which was associated with a 80% increase in pulse frequency and a 70% increase in pulse amplitude. Immunoreactive alpha-subunit secretion was also pulsatile before and after clomiphene treatment. Mean alpha-levels rose 70%, together with a 39% increase in pulse frequency and a 41% increase in pulse amplitude. Circulating testosterone and estradiol levels increased 2-fold and FSH levels increased 3-fold after clomiphene treatment. Insofar as each LH and uncombined alpha-subunit pulse reflects a LHRH secretory episode, our data indicate that endogenous estrogens tonically restrain the hypothalamic release of LHRH. From these results and those of previous studies, we conclude that estrogens as well as androgens are important in the testicular feedback inhibition of the hypothalamic oscillator that governs pulsatile gonadotropin secretion.


J Androl 1991 Jul-Aug;12(4):258-63

The effects of normal aging on the response of the pituitary-gonadal axis to chronic clomiphene administration in men.

Tenover JS, Bremner WJ.

Department of Medicine, University of Washington School of Medicine, Seattle.

Serum androgens decline with age in normal men, despite normal or elevated bioactive serum gonadotropins, suggesting that primary testicular dysfunction occurs with aging. The authors further assessed the question of age-related testicular dysfunction by evaluating whether raising serum gonadotropins above the normal serum range for an extended time in healthy elderly men might result in bringing their gonadal function to a level similar to that found in young adult men. Five elderly (65 to 85 years old) and five young adult men (26 to 33 years old) were given 50 mg of clomiphene citrate (CC) twice a day for 8 weeks to stimulate gonadotropin production. During that time, testosterone (T), non-sex hormone-binding globulin bound T, and estradiol increased significantly in both age groups, while serum inhibin increased significantly only in the young adult men. The increases in serum androgens with CC administration were significantly greater in the young adult men than in the elderly men. These hormone changes occurred in the setting of serum gonadotropins that increased significantly in both age groups, although there was a tendency for the elderly men to have a smaller increase in luteinizing hormone. Despite 8 weeks of stimulation of the pituitary-gonadal axis by CC administration, the elderly men demonstrated significantly diminished testicular responses compared with the young adult men. Sertoli cell function, as determined by inhibin production, was more diminished in the elderly men than was Leydig cell function. These data strengthen the hypothesis that normal aging in men is accompanied by a decline in testicular function.


Urology 1991 Oct;38(4):317-22

Possible hypothalamic impotence. Male counterpart to hypothalamic amenorrhea?

Guay AT, Bansal S, Hodge MB.

Section of Endocrinology, Lahey Clinic Medical Center, Burlington, Massachusetts.

Twenty-one men with erectile complaints who were found to have a low level of serum testosterone without a reciprocal elevation of the serum levels of luteinizing hormone were evaluated to identify whether the defect was of hypothalamic or of pituitary origin. Patients underwent a luteinizing hormone (LH)-follicle-stimulating hormone (FSH)-releasing hormone stimulation test that showed a normal but sluggish increase in LH and FSH levels, thus ruling out a pituitary defect and suggesting a suprapituitary abnormality. This was confirmed when, in response to clomiphene, patients had a normal increase in gonadotropin and testosterone levels. Although the basal as well as clomiphene and gonadotropin releasing hormone-stimulated levels of total testosterone and gonadotropins were identical in men less than and more than fifty years old, the elevation of free testosterone levels in response to clomiphene was higher in patients younger than fifty. This suggested that although the primary abnormality found in these patients is altered secretion of gonadotropin hormone-releasing hormone from the hypothalamus, an age-related decline in the responsivity of Leydig cells to LH may make it more manifest in older patients. Elevation of testosterone levels from a subnormal to a normal range in response to clomiphene administered for seven days suggests that the defect is functional and reversible and that the drug may be useful in treatment of sexual dysfunction in this group of patients.
Nephron 1993;63(4):390-4

Effect of clomiphene citrate on hormonal profile in male hemodialysis and kidney transplant patients.

Martin-Malo A, Benito P, Castillo D, Espinosa M, Burdiel LG, Perez R, Aljama P.

Department of Nephrology, Hospital Universitario Reina Sofia, Cordoba, Spain.

The aim of this study was to evaluate the role of clomiphene citrate (CC) therapy in the hypothalamus-pituitary-gonadal axis of male uremic subjects. Thirty-four patients on hemodialysis (HD) and 8 successful kidney transplant subjects (RT) were evaluated. Nine healthy males were used as controls ©. At baseline, zinc, testosterone (TEST), prolactin (PRL), FSH, LH and estradiol plasma concentrations were measured. All subjects were treated with CC (100 mg/day) for a week. The aforementioned parameters were determined again on the seventh day of CC therapy, and 3 days after drug withdrawal. Following CC, there was a rise in FSH, LH and TEST levels in all subjects (p < 0.05); it is interesting to stress that TEST became normal in HD. In addition, we observed a decrease of PRL after CC only in HD patients (p < 0.01). In summary, CC was able to partially correct most of the



Tamoxifen

nolvadex aka tamoxifen studies:

Arch Gynecol Obstet 1993;252(3):143-7

Tamoxifen treatment of oligozoospermia: a re-evaluation of its effects including additional sperm function tests.

Sterzik K, Rosenbusch B, Mogck J, Heyden M, Lichtenberger K.

Abteilung Frauenheilkunde, Geburtshilfe der Universitat, Ulm, Germany.

Because of previous contradictory results, we reevaluated the effects of tamoxifen on 29 men presenting with idiopathic oligozoospermia. To determine whether a possible increase in sperm concentration might be correlated with an improvement of sperm quality, the hamster ovum penetration (HOP) test and the hypo-osmotic swelling (HOS) test were included as additional tests of sperm function. Patients were treated with tamoxifen (20 mg/day) for 3 months. From 4 weeks until the end of the study, tamoxifen had no significant effect (P > 0.05) on blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), or estradiol (E2). There was no significant improvement (P > 0.05) of conventional semen parameters (volume, concentration, motility, morphology), and of HOP and HOS test results. The lack of correlation between a rise in hormone levels and improvement of sperm quality suggests that tamoxifen is of questionable value in men with idiopathic oligozoospermia.


Asian J Androl 2001 Jun;3(2):115-9

Effect of intermittent treatment with tamoxifen on reproduction in male rats.

Gill-Sharma MK, Balasinor N, Parte P.

Department of Neuroendocrinology, Institute for Research in Reproduction, ICMR, Parel, Mumbai, India. dirirr@vsnl.com

AIM: To identify the antifertility effect of intermittent oral administration of tamoxifen in male rat. METHODS: Tamoxifen was administered orally at a dose of 0.4 mg x kg(-1) x d(-1) with an intermittent regime for 120 days. Treated and control rats were mated with cycling female rats on days 60, 90 and 120 of treatment. The mated males were sacrificed and the weights of reproductive organs were recorded, and the serum levels of LH, FSH, testosterone and estradiol estimated by radioimmunoassay. In the female rats, the numbers of implantation sites, corpora lutea, and numbers of normal and resorbed foetuses were recorded on d 21 of gestation. The potency, fecundity, fertility index, litter size and post-implantation loss were then calculated. RESULTS: The fecundity of male rats was completely suppressed by tamoxifen while the potency was maintained at the control level. The fertility index was significantly decreased. No viable litters were sired. Post implantation loss, indicative of non-viable embryos, was observed but was not significantly increased above the control level. The weights of the testes, epididymides, ventral prostate and seminal vesicles were significantly reduced. The blood LH and testosterone levels were significantly decreased, but not FSH and estradiol. CONCLUSION: Intermittent oral tamoxifen administration completely suppressed the fecundity of adult male rats with reserved potency.


Case study showing benefit to FSH, LH, and testosterone from tamox- Notice administration duration

Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC Köksal IT Tunç M Nane I Tellaloglu S

[see related articles]

PrintEmail
--------------------------------------------------------------------------------

Affiliation
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.

Abstract
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy. PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment. RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant. CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.



Study between tamox administration and placebo- attention to highlighted

Int J Androl. 1992 Feb;15(1):14-8. Related Articles, Links


Comment in:
Int J Androl. 1992 Dec;15(6):507-8.

Treatment of idiopathic oligozoospermia with tamoxifen--a randomized controlled study.

Krause W, Holland-Moritz H, Schramm P.

Department of Andrology, Philipps-Universitat, Marburg, Germany.

There is no conclusive evidence of the usefulness of tamoxifen in the treatment of idiopathic oligozoospermia (OAT-syndrome), as it has been used mostly in uncontrolled studies. We herein report on the controlled treatment of OAT-syndrome with tamoxifen versus placebo following a randomized design. Seventy-six men with sperm counts of 2-20 x 10(6) ml-1, sperm motility of 20-50%, and sperm morphology (abnormal cells) between 50 and 80% were involved in the study. Patients with varicocele, a history of testicular maldescent or genital inflammation were excluded. Thirty-nine patients received tamoxifen (30 mg daily), 37 patients placebo. There was a statistically significant increase in the mean serum testosterone level after treatment in the tamoxifen-treated group (from 4.9 +/- 1.9 to 7.9 +/- 3.6 ng ml-1) in comparison to the placebo group (5.3 +/- 2.0 and 5.6 +/- 2.0 ng ml-1). Serum FSH levels increased slightly in the tamoxifen group (from 6.8 +/- 4.1 to 7.3 +/- 4.8 mU ml-1), but this was not statistically significant in comparison to the placebo group (from 5.9 +/- 3.9 to 5.2 +/- 3.5 mU ml-1). Serum levels of LH did not show any differences between groups. The sperm count increased during treatment from 9.3 +/- 11.7 to 11.4 +/- 13.7 x 10(6) ml-1 in the tamoxifen group and from 9.1 +/- 7.1 to 9.3 +/- 8.8 x 10(6) ml-1 in the placebo group; this difference did not reach statistical significance. The percentage of motile and abnormal sperm was not different between the two treatment groups



Study on benefit of tamox

again pay attention to duration. Also notice levels were checked at 2wks-12wks, but it is not specified when increased levels of FSH, LH, and T were seen at maximized effect. Levels of T and FSH are only significant, with T at miniscuel proportions

Fertil Steril. 1983 May;39(5):700-3. Related Articles, Links


Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.

Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.

Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.

[LuvMuhRoids]

Description
Bromocriptine ( broe-moe-KRIP-teen) belongs to the group of medicines known as ergot alkaloids. Bromocriptine blocks release of a hormone called prolactin from the pituitary gland. Prolactin affects the menstrual cycle and milk production. Bromocriptine is used to treat certain menstrual problems or to stop milk production in some women or men who have abnormal milk leakage. It is also used to treat infertility in both men and women that occurs because the body made too much prolactin.

Bromocriptine is also used to treat some people who have Parkinson's disease. It works by stimulating certain parts of the brain and nervous system that are involved in this disease.

Bromocriptine is also used to treat acromegaly (overproduction of growth hormone) and pituitary prolactinomas (tumors of the pituitary gland).

Bromocriptine may also be used for other conditions as determined by your doctor.

Bromocriptine is available only with your doctor's prescription, in the following dosage forms:

Oral
Capsules (U.S. and Canada)
Tablets (U.S. and Canada)



Before Using This Medicine
In deciding to use a medicine, the risks of taking the medicine must be weighed against the good it will do. This is a decision you and your doctor will make. For bromocriptine, the following should be considered:

Allergies—Tell your doctor if you have ever had any unusual or allergic reaction to bromocriptine or other ergot medicines such as ergotamine. Also tell your health care professional if you are allergic to any other substances, such as foods, preservatives, or dyes.

Pregnancy—Bromocriptine is not generally recommended for use during pregnancy. However, bromocriptine can be used during pregnancy in certain patients who are closely monitored by their doctor.

Breast-feeding—This medicine stops milk from being produced.

Children—Studies of this medicine have been done only in teenagers over 15 years of age and adult patients. There is no specific information comparing use of bromocriptine in children with use in other age groups.

Teenagers—This medicine has been tested in a limited number of teenagers 15 years of age and older. In effective doses, the medicine has not been shown to cause different side effects or problems than it does in adults. Appropriate studies have not been done in teenagers younger than 15 years of age, and there is no specific information comparing use of bromocriptine in these teenagers with use in other age groups.
Older adults—Confusion, hallucinations, or uncontrolled body movements may be more likely to occur in elderly patients, who are usually more sensitive than younger adults to the effects of bromocriptine.

Other medicines—Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking bromocriptine, it is especially important that your health care professional know if you are taking any of the following:

Ergot alkaloids (dihydroergotamine [e.g., D.H.E. 45], ergoloid mesylates [e.g., Hydergine], ergonovine [e.g., Ergotrate], ergotamine [e.g., Gynergen], methylergonovine [e.g., Methergine], methysergide [e.g., Sansert])—Severe cases of high blood pressure have occurred with the use of bromocriptine. This may be made worse with the use of ergot alkaloids
Erythromycin (e.g., E.E.S. or Erytab) or
Risperidone (e.g., Risperdal) or
Ritonavir (e.g., Norvir)—Use of these medications with bromocriptine may greatly increase the effects of bromocriptine

Other medical problems—The presence of other medical problems may affect the use of bromocriptine. Make sure you tell your doctor if you have any other medical problems, especially:
High blood pressure (or history of) or
Pregnancy-induced high blood pressure (history of)—Rarely, bromocriptine can make the high blood pressure worse
Liver disease—Toxic effects of bromocriptine may occur in patients with liver disease because the body is not able to remove bromocriptine from the bloodstream as it normally would
Mental problems (history of)—Bromocriptine may make certain mental problems worse



Proper Use of This Medicine
If bromocriptine upsets your stomach, it may be taken with meals or milk. Also, taking the dose at bedtime may help to lessen nausea if it occurs. If stomach upset continues, check with your doctor. Your doctor may recommend that you take the first doses vaginally.

Dosing—

The dose of bromocriptine will be different for different patients. Follow your doctor's orders or the directions on the label. The following information includes only the average doses of bromocriptine. If your dose is different, do not change it unless your doctor tells you to do so.

The number of capsules or tablets that you take depends on the strength of the medicine. Also, the number of doses you take each day, the time allowed between doses, and the length of time you take the medicine depend on the medical problem for which you are taking bromocriptine.

For oral dosage forms (capsules and tablets):
For infertility, male hormone problem (male hypogonadism), starting the menstrual cycle (amenorrhea), or stopping abnormal milk secretion from nipples (galactorrhea):
Adults and teenagers 15 years of age or older—At first, 1.25 to 2.5 milligrams (mg) once a day taken at bedtime with a snack. Then your doctor may change your dose by 2.5 mg every three to seven days as needed. Doses greater than 5 mg a day are taken in divided doses with meals or at bedtime with a snack.
Teenagers less than 15 years of age and children—Use and dose must be determined by your doctor.
For lowering growth hormone (acromegaly):
Adults and teenagers 15 years of age or older—At first, 1.25 to 2.5 milligrams (mg) once a day taken at bedtime with a snack for three days. Then your doctor may change your dose by 1.25 or 2.5 mg every three to seven days as needed. Doses greater than 5 mg are divided into smaller doses and taken with meals or at bedtime with a snack.
Teenagers less than 15 years of age and children—Use and dose must be determined by your doctor.
For Parkinson's disease:
Adults and teenagers 15 years of age or older—At first, 1.25 milligrams (mg) one or two times a day taken with meals or at bedtime with a snack. Then your doctor may change your dose over several weeks as needed.
Teenagers less than 15 years of age and children—Use and dose must be determined by your doctor.
For pituitary tumors:
Adults and teenagers 15 years of age or older—At first, 1.25 milligrams (mg) two or three times a day taken with meals. Then your doctor may change your dose over several weeks as needed.
Teenagers less than 15 years of age and children—Use and dose must be determined by your doctor.
Missed dose—

If you miss a dose of this medicine and remember it within 4 hours, take the missed dose when you remember it. However, if a longer time has passed, skip the missed dose and go back to your regular dosing schedule. Do not double doses.

Storage—

To store this medicine:

Keep out of the reach of children.
Store away from heat and direct light.
Do not store in the bathroom, near the kitchen sink, or in other damp places. Heat or moisture may cause the medicine to break down.
Do not keep outdated medicine or medicine no longer needed. Be sure that any discarded medicine is out of the reach of children.


Precautions While Using This Medicine
It is important that your doctor check your progress at regular visits, to make sure that this medicine is working properly and to check for unwanted effects.

This medicine may cause some people to become drowsy, dizzy, or less alert than they are normally. Make sure you know how you react to this medicine before you drive, use machines, or do anything else that could be dangerous if you are dizzy or are not alert.

Dizziness is more likely to occur after the first dose of bromocriptine. Taking the first dose at bedtime or when you are able to lie down may lessen problems. It may also be helpful if you get up slowly from a lying or sitting position. Your doctor may also recommend that you take the first dose vaginally.

Bromocriptine may cause dryness of the mouth. For temporary relief, use sugarless candy or gum, melt bits of ice in your mouth, or use a saliva substitute. However, if dry mouth continues for more than 2 weeks, check with your medical doctor or dentist. Continuing dryness of the mouth may increase the chance of dental disease, including tooth decay, gum disease, and fungus infections.

It may take several weeks for bromocriptine to work. Do not stop taking this medicine or reduce the amount you are taking without first checking with your doctor.

Drinking alcohol while you are taking bromocriptine may cause you to have a certain reaction. Avoid alcoholic beverages until you have discussed this with your doctor. Some of the symptoms you may have if you drink any alcohol while you are taking this medicine are blurred vision, chest pain, confusion, fast or pounding heartbeat, flushing or redness of face, nausea, severe weakness, sweating, throbbing headache, or vomiting.

For females who are able to bear children and who are taking this medicine for menstrual or infertility problems, to stop milk production, or to treat acromegaly or pituitary tumors:

It is best to use some type of birth control while you are taking bromocriptine. However, do not use oral contraceptives (“the Pill”) since they may prevent this medicine from working. For women using bromocriptine for infertility, tell your doctor when your normal menstrual cycle returns. If you wish to become pregnant, you and your doctor should decide on the best time for you to stop using birth control. Tell your doctor right away if you think you have become pregnant while taking this medicine. You and your doctor should discuss whether or not you should continue to take bromocriptine during pregnancy.
Check with your doctor right away if you develop blurred vision, a sudden headache, or severe nausea and vomiting.


Side Effects of This Medicine
Along with its needed effects, a medicine may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.

Some serious side effects have occurred during the use of bromocriptine to stop milk flow after pregnancy or abortion. These side effects have included strokes, seizures (convulsions), and heart attacks. Some deaths have also occurred. You should discuss with your doctor the good that this medicine will do as well as the risks of using it.

Check with your doctor immediately if any of the following side effects occur:

Rare
Black, tarry stools; bloody vomit; chest pain (severe); convulsions (seizures) ; fainting; fast heartbeat ; headache (unusual); increased sweating; nausea and vomiting (continuing or severe) ; nervousness; shortness of breath (unexplained); vision changes (such as blurred vision or temporary blindness); weakness (sudden)


Check with your doctor as soon as possible if any of the following side effects occur:

Less common—reported more often in patients with Parkinson's disease
Confusion; hallucinations (seeing, hearing, or feeling things that are not there); uncontrolled movements of the body, such as the face, tongue, arms, hands, head, and upper body


Rare—reported more often in patients taking large doses
Abdominal or stomach pain (continuing or severe); increased frequency of urination; loss of appetite (continuing); lower back pain; runny nose (continuing); weakness


Other side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. However, check with your doctor if any of the following side effects continue or are bothersome:

More common
Dizziness or lightheadedness, especially when getting up from a lying or sitting position; nausea


Less common
Constipation; diarrhea; drowsiness or tiredness; dry mouth; leg cramps at night; loss of appetite ; mental depression; stomach pain; stuffy nose; tingling or pain in fingers and toes when exposed to cold; vomiting


Some side effects may be more likely to occur in patients who are taking bromocriptine for Parkinson's disease, acromegaly, or pituitary tumors since they may be taking larger doses.

Other side effects not listed above may also occur in some patients. If you notice any other effects, check with your doctor.



Additional Information
Once a medicine has been approved for marketing for a certain use, experience may show that it is also useful for other medical problems. Although these uses are not included in product labeling, bromocriptine is used in certain patients with the following medical conditions:

To stop milk production after an abortion or miscarriage or in women after a delivery who should not breast-feed for medical reasons
Neuroleptic malignant syndrome

[LuvMuhRoids]

Problem with Tren and Deca is suffering prolactin affects unlike the estrogen unbalance from using test products like enanthate or cypionate and suffering inflamation of the mammory glands. Tren/Deca cause prolactin levels to raise and suffer secretion of the nipples. With nandrolones and there derivatives like Deca and Tren comes the risk of raising prolactin levels in the body to such a high level that lactation may begin to occur from the nipple. This is known as Galactorrhea and not Gynocomastia.

This is why bromocriptine is used. It is a prolactin inhibitor. B6 is also used because it suppresses prolactin levels as well. B6 should be used first rather than bromo. There are sides with bromo unlike with using B6. Doses of 200mg ed of b6 would be sufficient to suppress prolactin levels, and a dose of 2.5mg split in the day and evening(1.25am/1.25pm) of bromo will suffice for prolactin inhibition.

Bromo should be used as a last resort if dosage of 200-600mg of B6 ED are not sufficient to subside these prolactin affects.

[LuvMuhRoids]

The Axis

The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body’s natural production of testosterone. Too much testosterone and the furnace will shut off. Not enough, and the heat is turned up, to put it very simply. For the purposes of our discussion here we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed. Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

[LuvMuhRoids]

This is an article I resort to often in advicing on HCG usage. I have read many studies on this product and its abilities. I would like to note that HCG is not to be mistaken for a suppliment to clomid or nolavdex for PCT. HCG tricks the testes into reproduction by mimicing LH. It does not restore the HPTA to a proper recovery. This is only accomplished by clomid/nolvadex therapy. HCG can not be used together in conjuction with clomid for one inhibits the other. I have read users administering HCG right after a cycle for a quick restore then start clomid therapy right after. It should only be used to cure symptoms of "testicular atrophy".

LMR


Nick and Bigfella - MuscleTalk.co.uk moderators

Using HCG
It is our opinion that HCG is probably one of the most misunderstood and misused compounds in bodybuilding. Hopefully this information will go some way towards rectifying that for the members of MuscleTalk. HCG stands for Human Chorionic Gonadotrophin and is not a steroid, but a natural peptide hormone which develops in the placenta of pregnant women during pregnancy to controls the mother's hormones. (Incidentally, this is the reason you may hear of people testing for growth hormone (HGH) with a pregnancy testing kit - If their HGH shows 'pregnant', they've been ripped-off with cheaper HCG - but we digress slightly).

Its action in the male body is like that of LH, stimulating the Leydig cells in the testes to produce testosterone even in the absence of endogenous LH. HCG is therefore used during longer or heavier steroid cycles to maintain testicular size and condition, or to bring atrophied (shrunken) testicles back up to their original condition in preparation for post-cycle Clomid therapy. This process is necessary because atrophied testicles produce reduced levels of natural testosterone, this situation should be rectified prior to post-cycle Clomid therapy.

HCG administration post-cycle is common practice among bodybuilders in the belief that it will aid the natural testosterone recovery, but this theory is unfounded and also counterproductive. The rapid rise in both testosterone, and thus oestrogen due to aromatisation, from the administration of HCG causes further inhibition of the HPTA (Hypothalamic/Pituitary/Testicular Axis - feedback loop discussed above); this actually worsens the recovery situation. HCG does not restore the natural testosterone production.

The typically observed dosing of 2000 to 5000IU every 4 to 5 days causes such an increase in oestrogen levels via aromatisation of the natural testosterone that this has been responsible for many cases of gynecomastia.

From the above discussion it is clear that HCG is best used during a cycle, either to:

1) Avoid testicular atrophy, or
2) Rectify the problem of an existing testicular atrophy.

Doses of HCG
Smaller doses, more frequently during a cycle will give best overall results with least unwanted side effects. Somewhere between 500iu and 1000iu per day would be best over about a two-week period. These doses are sufficient to avoid/rectify testicular atrophy without increasing oestrogen levels too dramatically and risking gynecomastia. This dosing schedule also avoids the risk of permanently down-regulating the LH receptors in the testes.

Presentation and Administration of HCG
Synthetic HCG is often known as Pregnyl (generic name) and is available in 2500iu and 5000iu (not ideal for the above doses!). Administration of the compound is either by intra-muscular or subcutaneous injection. It comes as a powder which needs to be mixed with the sterile water. The powder is temperature-sensitive prior to mixing and should not be exposed to direct heat. After mixing, it should be kept refrigerated and used within a few weeks - though there are sterility issues which need to be considered after mixing.

Summary and Price of Clomid and HCG
Clomid is more effective than HCG post cycle, but some long-term users like to use HCG during a cycle, or to prepare the testes for Clomid therapy.

Clomid is available in 50mg tablets most commonly, but also comes in 25mg capsules. 10 x 50mg tablets should be anywhere from £10-20; $10 - $20.00. HCG prices range from £15-£25 per 3 ampoules.

http://www.muscletalk.co.uk/clomid-hcg.asp



HCG is provided as a glycoprotein powder to be diluted with water, and acts in the body like LH, stimulating the testes to produce testosterone even when natural LH is not present or is deficient. It therefore is useful for maintaining testosterone production and/or testicle size during a steroid cycle. Use of this drug in the taper is rather counterproductive, since the resulting increased testosterone production is itself inhibitory to the hypothalamus and pituitary, delaying recovery. Thus, if this drug is used, it is preferably used during the cycle itself. A daily amount of 500 IU is generally sufficient, and in my opinion usage should not exceed 1000 IU per day.

Daily administration is superior to less frequent administration.

Doses over 1000 IU are noted for their tendency to cause or aggravate gynecomastia, and also act to desensitize the testicles to LH.

HCG may be injected intramuscularly, subcutaneously, or in a shallow injection about 1/4" deep with the needle going straight in. A 29 gauge insulin needle is recommended. Injection speed should be slow.

Some HCG products are diluted 5000 or even 10,000 IU per mL, while others are diluted 1000 IU per mL. So far as I know there is no need to make the preparation so dilute. Once mixed, the preparation should be refrigerated and used within a few weeks. The substance is also somewhat temperature sensitive before mixing and should not be exposed to excessive heat.

HCG does not correct the problem of progressively-decreasing ejaculatory volume that is typical during a steroid cycle. So far as I know the only cure is to go off-cycle and use Clomid, but it is possible that HMG, a related drug which works analogously to FSH might be useful during a cycle to treat this problem. HMG supports spermatogenesis and is commonly used in conjunction with HCG to treat male fertility problems. (Consider use of HMG to maintain ejaculatory volume to be a strictly past-the-cutting-edge hypothesis: I have not yet had the opportunity to test the matter.)

The athlete who would otherwise fail a urinary ratio test because of low epitestosterone may find HCG useful in increasing epitestosterone and therefore improving this ratio. A 500 IU dose is sufficient, but on the other hand, HCG itself is also banned by the IOC and is readily detected in urine.

HCG can also useful for returning testosterone to normal levels should levels be low post-cycle, or, with care, to increase levels from normal to high normal. Titration of the dose, by measuring T levels and then adjusting the HCG dose accordingly, is recommended for long term use.

[LuvMuhRoids]

Below you'll find starting times for your PCT based on the active life of each compound. The active life is the duration of time it takes for the exogenous hormone to be absorbed, utilized, and expelled; no longer being bioavailable. Keep in mind that active life is an approximation which is dependant on dose, ester, as well as the individuals metabolization of the compound ; but for the moderate user, these are as close to precise as you'll find.

Anadrol/Anapolan: 12 hours after last administration
Deca: 21 days after last injection
Dianabol: 12 hours after last administration
Equipoise: 21 days after last injection
Fina: 3 days after last injection
Primobolan depot: 14 days after last injection
Sustanon: 18 days after last injection
Testosterone Cypionate: 18 days after last injection
Testosterone Enanthate: 14 days after last injection
Testosterone Propionate: 3 days after last injection
Testosterone Suspension: 24 hours after last administration
Winstrol: 12 hours after last administration


Above is not my chart or comments but I would like to note for this chart. The timing for CYPIONATE is 18 days as opposed to 2 weeks like the chart I resort to. It is thought that cypionate is identical to enanthate but it is not. The half life of cypionate is just a little more than enanthate and start time is 18 days rather than 14 days as most had thought. This I find interesting and true.


LMR